The Dopamine Made Me Do It

Volkow’s interest in the chemistry and mechanisms of the brain began in Mexico City in 1981. She had just graduated from medical school and read an article in Scientific American about exciting new clinical applications of a technology called positron emission tomography (PET). PET allows scientists to see a three-dimensional image of the brain as it thinks, feels and works (previously, scientists could not watch the brain in action very well). Volkow was awestruck, and applied for a psychiatric residency at New York University to have a chance to work with nearby PET pioneers at the Department of Energy’s Brookhaven National Laboratory on Long Island.

She was particularly interested in the brains of people who lose the ability to control their actions rationally; people who, in essence, lose free will. At first, she studied schizophrenics. By the late 1980s, she started looking at the brains of alcoholics and drug addicts as well. She soon saw that the addicted brains looked decidedly different from brains of people without drug or alcohol addictions.

The most marked difference was in the dopamine cells of the reward circuit, a group of brain cells that communicate using the chemical dopamine. The circuit connects several regions in the brain involved in the feeling of reward, which has evolved to motivate us to do more of the things that make us feel good and are important for survival, like eating, having sex and taking care of children. Drugs like cocaine and amphetamines highjack this circuit, causing a flood of dopamine into the area between brain cells where messages are transmitted. And this dopamine surge produces a high. Take the drugs often enough and dopamine receptors can decrease in number or become less sensitive to dopamine. When this happens, a person needs more and more of the drug to get the same effect (this is called tolerance).

As a psychiatrist, Volkow noted a similarity between drug abusers and compulsive overeaters: they both seemed to lose their rational ability to control their behaviors (around drugs and food, respectively). She wanted to know how to intervene to help those who couldn’t stop themselves. She knew that antipsychotic drugs, which block the reward-registering dopamine system, often make people eat and gain weight (as a side effect), while drugs that increase dopamine in the brain cause weight loss. In 2001, Volkow and her colleagues began exploring whether dopamine played a key role in overeating and obesity in people not on drugs.

To find out, Volkow and her crew gave a radioactive chemical that binds to dopamine receptors to 20 people—10 obese, 10 normal weight—and then scanned their brains using PET, to see whether there were any associations between their dopamine systems and their body weights.

Turns out, there were. The obese people had significantly fewer dopamine receptors in a part of the brain called the striatum. Volkow and her team surmised that with fewer receptors, the people who were obese had to eat far more food than a normal-weight person to experience the same high.